The cellular foundation for complex neural processes, such as learning and memory, is thought to be the remarkable ability of neurons to modulate the efficacy of synaptic transmission. Dysregulation of synaptic plasticity contributes to the pathology of an array of neurological conditions. Despite their importance, the molecular mechanisms that regulate synaptic plasticity are poorly characterized. The proposed research will utilize the synaptic immediate-early gene Arc as a molecular tool to investigate the mechanisms underlying this phenomenon. The specific aims of this proposal are: Specific Aim 1: Identify ERK-responsive promoter elements that underlie BDNF-mediated transcription of Arc mRNA. Specific Aim 2: Determine if ERK signaling is necessary and sufficient for TrkB-mediated translation of Arc. Specific Aim 3: Determine if TrkB-mediated PLCg signaling regulates Arc protein levels.